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Int J Clin and Biomed Res.

2016;2(4): 01-06
Journal homepage: www.ijcbr.com
INTERNATIONAL JOURNAL OF CLINICAL
AND BIOMEDICAL RESEARCH

Research article

STUDY OF SERUM LIPID PROFILE AND FASTING BLOOD SUGAR IN POLYCYSTIC OVARIAN
SYNDROME
SADANANJALI1, SREEKANTHA2, H AMRUTH*3

ABSTRACT
*TINKAL
ARTICLE PATEL
INFO

Received: 4th July 2016


Revised 25th July 2016
Accepted: 5th Aug 2016
AUTHOR DETAILS
1

Postgraduate, 2Proffessor & HOD,


Department of Biochemistry, Raichur
Institute of Medical Sciences, Raichur584102.
3

Medical officer, Health & Family welfare


Department, Gulbarga-585102.

*Corresponding author email:


hukkeri.amruth@gmail.com

Background: Polycystic ovarian syndrome (PCOS) is the multisystemic disorder


and most common reproductive endocrinopathy of women during their
childbearing years, expressed in wide varieties of clinical signs and symptoms. It is
characterized by a varied and often complex array of metabolic and endocrine
abnormalities, including hyperinsulinaemia, hyperglycaemia, glucose intolerance
and obesity which put women with PCOS at a higher risk for diabetes,
hypertension, dyslipidemia, and cardiovascular disease. Objectives: To estimate
Fasting blood glucose and lipid profile in women with PCOS and normal females.
Materials and Methods: After Ethical Committee Approval, blood samples were
collected from 50 diagnosed PCOS cases and 50 healthy controls (premenopausal
women); aged 18 to 40 years. Fasting plasma glucose and lipid profile were
investigated in both PCOS patients and controls. The correlation between these
biochemical parameters were then studied in the PCOS group. Data analysis done
using student t test. Result: There was a significant increase in fasting plasma
glucose levels in PCOS patients as compared to controls. PCOS women had higher
BMI with increased total cholesterol, TGL, LDL-C, VLDL-C and lower HDL-C (P <
0.05) as compared to the controls which was statistically significant. The levels of
glucose showed significant positive correlation with total cholesterol(P<0.01),
triglycerides(P<0.05), LDL-C (P<0.01) whereas non-significant negative correlation
with HDL-C. Conclusion: The findings of this study confirms the association
between Glucose, BMI and dyslipidaemia in PCOS and may help to identify
women with PCOS at risk of cardio metabolic syndrome thereby confirming the
association between PCOS and cardiovascular risk factors.
Keywords: Polycystic Ovarian Syndrome, Dyslipidaemia, Cardio Metabolic
Syndrome, Insulin Resistance.

INTRODUCTION
Polycystic ovarian syndrome (PCOS) is the multisystem
reproductive endocrinopathy with ovarian expression
of metabolic disturbances and a wide spectrum of
clinical features characterized by increased ovarian and
adrenal
androgen
secretion,
hyperandrogenic
metabolic syndrome symptoms such as hirsutism, acne
and/or alopecia, menstrual irregularity and polycystic
ovaries. It is not only a reproductive endocrinopathy
but also a metabolic disorder.[1,2]
The exact prevalence of PCOS is not known as the
syndrome has not been precisely defined. The
estimated prevalence in women of reproductive age is
5-10%.[3]The pathophysiology is complex involving the
hypothalamus-pituitary-ovarian axis, ovarian theca cell
H AMRUTH et al.

hyperplasia, hyperinsulinemia and a multitude of other


cytokine and adipocyte-driven factors.[4]
Women with PCOS share many features in common
with the metabolic syndrome[1] and It is also associated
with an increased risk for metabolic complications like
insulin resistance (IR) with consequent compensatory
hyperinsulinaemia, dyslipidaemia and cosmetic
problems.[5]One of the most prominent metabolic
symptoms of PCOS is insulin resistance, which includes
hyperinsulinaemia and impaired glucose tolerance.They
also develop abnormal glucose metabolism at a
younger age and may demonstrate a more rapid
conversion from impaired glucose tolerance to type2
diabetes mellitus.[6]Impaired glucose tolerance and
diabetes are not only known risk factors for
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Int J Clin and Biomed Res. 2016;2(4): 01-06

cardiovascular disease but also present with their own


morbidity.
Obesity increases hyperandrogenism, hirsutism,
infertility and pregnancy complications both
independently and by exacerbating PCOS. Likewise, in
PCOS obesity worsens insulin resistance and
exacerbates
reproductive
and
metabolic
[7]
features. Adiposity plays a vital role in the
development and maintenance of PCOS and it strongly
influences the severity of both its clinical and endocrine
features. In addition to abnormal distribution of
adipose tissue in women with PCOS, there may also be
inherent abnormalities of lipolysis within adipocytes
that are site specific[8]. Women with PCOS have
disturbed lipid profiles. The causes of dyslipidaemia in
PCOS are again multifactorial. Insulin Resistance
appears to have a important role; mediated in part by
stimulation of
lipolysis and altered expression of
lipoprotein lipase and hepatic lipase.[9]
IR and dyslipidemia seem to have an important role on
the risk of cardiovascular pathology in women with
PCOS. It is still not known to what degree dyslipidemia
contributes to this risk.[10]
PCOS may represent the largest under-appreciated
segment of the female population at risk of Type2
Diabetes Mellitus and cardiovascular disease. So, it is
recommended that women with PCOS be routinely
screened for indicators of early metabolic changes in
order to anticipate early diagnosis and management. In
view of this, the present study was undertaken to
estimate and correlate the fasting blood sugar levels
and lipid profile that may help to identify women with
PCOS at risk of Cardiometabolic syndrome.

MATERIAL AND METHODOLOGY


The observational case-control study was conducted at
Raichur institute of medical sciences teaching Hospital,
and OPEC super specialty Hospital Raichur from
September 2014-September 2015. Study consists of 50
female patients newly diagnosed with PCOS based on
Rotterdam criteria in the age group of 18-40 years as
cases and 50 age matched healthy female volunteers
with regular menstrual cycles and with no clinical
evidence of hyperandrogenism or PCOS were taken as
control subjects. Institutional ethical committee
approved the study and informed consent obtained
from all the study subjects. All subjects answered a
questionnaire which contained details of age,
H AMRUTH et al.

menstrual history, medical history and family history of


type2 diabetes mellitus or polycystic ovarian syndrome.
Inclusion criteria:
Cases: Female patients newly diagnosed with PCOS
based on Rotterdam Criteria, in the age group of 18-40
years.
Women
with
oligomenorrhoea/Amenorrhoea,
clinical/Biochemical signs of hyperandrogenism
(including: Hirsutism, Acne, Alopecia etc.), elevated
androgen levels, Presence of Polycystic ovaries on USG
were included in the study.
Controls: Age matched healthy female volunteers with
regular menstrual cycles and no signs of clinical
hyperandrogenism or PCOS.
Exclusion criteria:
Women with Diabetes mellitus, hypertension, thyroid
disorders, renal diseases, cardiovascular diseases,
cushing syndrome, pregnant/lactating women, women
on drugs (oral contraceptives, hypoglycemic agents/
lipid lowering drugs), hormonal medicines within 6
weeks were excluded from the study.
Method of collection of data:
A pre-structured and pretested proforma was used to
collect the data. Baseline data including age, BMI,
detailed medical history, family history, clinical
examinations were included as part of the
methodology.
Anthropometric data:
Body Mass Index:
All the subjects height and weight were recorded using
standard apparatus.
Body mass index (BMI) was calculated by dividing
weight (kg) by height (m2).
Normal weight was defined as BMI < 25, Overweight as
BMI between 25.0-29.9 and Obesity as BMI > 30.
Waist circumference and waist:hip ratio
Waist circumference was measured mid-way between
the last palpable rib and the top part of the iliac crest
and the hip circumference was taken around the widest
portion of the buttocks.
Blood Pressure:
Blood Pressure was measured in the right arm, with the
subjects in a relaxed sitting position using a mercury
sphygmomanometer.
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Int J Clin and Biomed Res. 2016;2(4): 01-06

Sample Collection and Storage:


5 ml of venous blood samples was collected from
healthy controls and women with PCOS after 12 hrs
overnight fast. 1 ml of sample was taken in a tube
containing anticoagulant and analysed for plasma
glucose. 4 ml of sample was taken in a plain tube. After
centrifugation at 3000 rpm for 10 minutes, the serum
samples were incubated for 15 minutes at room
temperature and analysed.
Biochemical Method:
Lipid Profile using standard kits (ERBA: Glucose,TotalCholesterol, Triglycerides, High Density LipoproteinCholesterol [HDL-C]) in Semi- Auto analyser (Mannheim
Erba chem5X) either on the same day of collection or
stored at 2-80C until further analysis.
I. Plasma glucose was analysed by Glucose OxidasePeroxidase Method
II. Serum sample was used for following biochemical
assays:
Lipid Profile:
Total Cholesterol (Cholesterol Oxidase Method);
Triglycerides (Glycerol Phosphate Oxidase and
Peroxidase Method);
High Density Lipoprotein Cholesterol (Phosphotungstic
Acid Method);
LDL-C and VLDL-C were calculated using the
Friedewalds formula:
LDL Cholesterol = [Total cholesterol] - [HDL cholesterol]
[TRIGLYCERIDE]/5;
VLDL Cholesterol = [Triglyceride]/5 (Where all
concentrations are given in mgs/dl)
Statistical Analysis: Data Analysis was performed using
SPSS 16 Software. The values were expressed as mean
Standard Deviation. Deviation and the findings were
analysed by student t test. Pearson's correlation
coefficients were calculated to assess the correlation
between the biochemical parameters in the study
group. A 'P' value of < 0.05 was considered statistically
significant.

RESULTS
Table I shows the mean, standard deviation and P
values of anthropometric measurement, FBS and Lipid
profile in PCOS patients and controls. The mean age of
the PCOS group and the control group were not
statistically significant. PCOS patients had significantly
high BMI (p < 0.01), waist circumference (p<0.001),
Systolic Blood Pressure (P<0.001) and diastolic blood
pressure (P < 0.001) as compared to controls.
H AMRUTH et al.

The PCOS group showed a significantly higher fasting


glucose (P < 0.001). PCOS patients had increased total
cholesterol, triglycerides, LDL-C, VLDL-C and decreased
HDL-C as compared to the controls which were
statistically significant.
Table : shows correlation between various parameters
in PCOS cases. From the table it can be inferred that
BMI (kg/m2) has significant positive correlation with
Fasting blood glucose, total cholesterol, triglyceride,
LDL-c and VLDL-c where as significant negative
correlation with HDL-c. From the table it can be
inferred that Fasting blood sugar level has significant
positive correlation with serum total cholesterol, serum
triglyceride, serum LDL-c and serum VLDL-c whereas
non significant negative correlation with serum HDL-c.
Table 1. Mean, Standard Deviation and P Values of
Anthropometric Measurements, Fasting blood sugar and
Lipid profile in PCOS Patients and Control Groups.
Parameter

Cases (n=50)

Controls(n=50)

P
value

Age (yrs)

26.16 3.77

27.38 5.01

>0.05

BMI (Kg/m2)

27.50 2.54

25.9 2.21

<0.01

Waist
circumference

85.47 5.46

78.24.34

<0.001

Waist Hip ratio

0.786 0.055

0.73840.05

>0.05

SBP (mm Hg)

118.488.79

110.965.92

<0.001

DBP (mmHg)

78.925.47

74.524.19

<0.001

FBS (mg/dl)

97.62 7.19

90.28 8.52

<0.001

165.52 19.21

<0.001

(cm)

Total cholesterol

187.4425.08

(mg/dl)

Triglyceride

138.3 40.32

104.69 32.88

<0.01

HDL-c (mg/dl)

40.64 8.87

45.78 5.86

<0.05

LDL-c (mg/dl)

120.17 28.17

98.79 19.45

<0.001

VLDL-c (mg/dl)

27.61 8.91

20.936.57

<0.01

(mg/dl)

P value of <0.05 considered statistically significant

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Table 2. correlation of BMI with other parameters in PCOS

BMI(kg/m2)

Parameter
r

Glucose

0.687

<0.01

Total cholesterol

0.691

<0.01

Triglyceride

0.568

<0.01

HDL-c

-0.391

<0.05

LDL-c

0.607

<0.01

VLDL-c

0.498

<0.01

P value of <0.05 considered statistically significant


Table 3. Correlation of Glucose and Lipid profile in PCOS

Parameter

Glucose (mg/dl)
r

Total cholesterol

0.740

<0.01

Triglyceride

0.377

<0.05

HDL-c

-0.251

>0.05

LDL-c

0.699

<0.01

VLDL-c

0.321

<0.05

P value of <0.05 considered statistically significant

DISCUSSION
Considerable evidence has accumulated for the
coexistence of the metabolic syndrome and PCOS. A
key alteration in the former appears to be insulin
resistance which is associated with an increased
morbidity and mortality due to coronary artery disease
with its enormous public health implications. It has
been suggested that inherited defects leading to
peripheral insulin resistance and concurrent
hyperinsulinaemia are among the causative factors for
the development of PCOS. However, due to the
heterogeneity of PCOS, it is unclear whether all subjects
with this disease are equally susceptible to the
symptoms and sequelae of the metabolic syndrome. All
in all, the possibility of an increased risk of coronary
artery disease in women with PCOS warrants effective
diagnostics of the syndrome. Known susceptibility to
coronary heart disease should also be kept in mind
when designing hormonal therapies for PCOS patients.
Clinical manifestations of the metabolic syndrome, i.e.
coronary artery disease and diabetes mellitus, have
H AMRUTH et al.

caused it to be referred to as the 'secret killer'. As


preventive measures can slow down the appearance of
these late symptoms, it is important to recognize at-risk
populations during the symptomless period[11]. Cardio
metabolic syndrome is a clustering of inter related risk
factors that promote the development of
atherosclerotic vascular disease and Type 2 DM. These
interrelated risk factors have direct effect on
atherogenic Dyslipidaemia, elevated blood pressure,
and elevated plasma glucose, and promote
proinflammatory and prothrombotic states.[12]
Obesity is defined as BMI of > 30 and overweight as
BMI of 25-29.9. PCOS patients display central or
abdominal or android obesity, which is characterized by
an increased waist-hip ratio. This visceral distribution of
adipose tissue can be inferred clinically by a waist-hip
ratio of more than 0.85.In our study the mean BMI in
normal healthy women (controls) is 25.92.21(kg/m2)
and in PCOS women (cases) is 27.502.54(kg/m2). The
mean BMI was higher in PCOS cases than controls and
the mean difference was statistically significant
(P<0.01). This is in accordance with other study which
showed that excess visceral fat seems to be predictive
not only of the metabolic syndrome but also of CVD. A
persons waist circumference is the simplest way to
assess central obesity. Waist circumference has been
shown to be one of the most accurate
anthropometrical indicators of abdominal fat.[13]Waist
circumference80 cm in women is considered as a
positive indicator of abdominal obesity as per the
consensus India guidelines for Indian population.[14] In
our study mean waist circumference for normal healthy
women (controls) is 78.24.34 cm and in PCOS
women(cases) is 85.475.46 cm and there was highly
significant statistical difference in the mean waist
circumference values (P<0.001). In the present study
the mean waist hip ratio for normal healthy women
(controls) is 0.73840.033 and in PCOS women (cases)
is 0.7860.0551. The mean waist hip ratio was higher in
cases than controls and the mean difference was not
statistically significant.
In our study mean systolic blood pressure in normal
healthy women (controls) is 110.965.992 mmHg and in
PCOS women(cases) it is 118.488.795 mmHg. The
mean diastolic blood pressure in controls is 74.524.19
mmHg and in cases it is 78.925.473 mmHg. There is
highly significant statistical difference in the mean
blood pressure values (P<0.001).
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Impaired glucose tolerance (IGT) AND impaired fasting


glucose (IFG) are now referred to as pre-diabetic
indicating the relatively high risk for development of
diabetes in these persons. In the absence of pregnancy,
IFG and IGT are not clinical entities in their own right
but rather risk factors for future diabetes as well as
cardiovascular diseases.[15
The results of our study showed mean fasting blood
glucose in normal healthy women (controls) as
90.288.52 mg/dl and in PCOS women (cases) it was
97.927.196 mg/dl. There was very highly significant
statistical difference in the mean fasting blood glucose
values (P<0.001). Our study also showed significant
positive correlation between fasting blood glucose and
BMI, TG and VLDL-c (P<0.05) and high significant
positive correlation with, TC and LDL-c (P<0.01)
whereas non significant negative correlation with HDL-c
(P>0.05).
V.M. Vinodhini et al., showed no statistically significant
differences in the mean concentrations of fasting
plasma glucose between PCOS patients and healthy
controls[16] whereas, a study by Azevedo MF et al.,
reported higher fasting glucose levels in PCOS women
which was statistically significant.[17]Our result was
consistent with the study of Azevedo MF et al.,. Our
study is consistant with the other study conducted
among 30 pre-menopausal women and 30 healthy
controls, increased fasting glucose levels and decreased
magnesium levels were noted in women with PCOS as
compared to controls and the differences noted were
statistically significant.[3]In another study, impaired
glucose tolerance (IGT), fasting insulin and Homeostasis
Model Assessment of IR (HOMA-IR) were found to be
significantly higher in the study group, when compared
to the healthy controls.[18]In a study conducted among
28 PCOS patients and 24 control women who were
divided into obese and non-obese groups, 75% of the
PCOS subjects presented with insulin resistance
suggesting that insulin resistance not only depends on
the BMI but also on the presence of PCOS.[19]
Obesity is known to have a strong influence on the
prevalence of several metabolic abnormalities in
women with PCOS. The syndrome may be associated
with a change in both lipid and lipoprotein metabolism
(a more atherogenetic lipoprotein pattern is seen in the
presence of obesity). Increase in the triglycerides and
total cholesterol levels and a greater reduction of highdensity lipoproteins (HDLs) have been observed in
H AMRUTH et al.

obese women with PCOS.[20]Our study showed highly


significant statistical difference in the mean values of
TC, TG, LDL-c and VLDL-c in PCOS cases than controls,
the mean values being higher in cases than controls
where as mean HDL-c values were lower in PCOS cases
than controls and the difference was statistically
significant. This is in agreement with the other study
which show that there is an elevation of triglycerides,
cholesterol and LDL-C in combination with decreased
HDL-C and apoA-I.3.
Our study found that HDL-C is lower in PCOS group than
in control group whereas higher mean VLDL was seen in
PCOS compared to controls. This is consistent with the
other study who showed that women with PCOS had
higher triglycerides and VLDL-C with lower HDL2-C and
apolipoprotein A1:A2 ratios.[21]
Another study compared lean and obese PCOS with
control subjects. They also found lower levels of HDL2
cholesterol and higher levels of apolipoprotein B in
PCOS. Obese women had lower levels of HDL-C and
apoA-I with higher triglycerides and VLDL-C.[22]A study
by AnuradhaKalra et al., found no correlation between
BMI with various lipid parameters.[2] But in our
investigation, we found a significant positive correlation
between BMI and total cholesterol, triglycerides, LDL-C,
VLDL-C and significant negative correlation between
BMI and HDL-C. Our study is in agreement with the
another study where the total serum cholesterol,
triglycerides, LDL cholesterol (LDL-C) and Very Lowdensity lipoprotein cholesterol(VLDL-C) were higher in
the women with PCOS and higher BMI. Significantly
lower levels of serum HDL-C were also noted. Positive
correlations were observed between: uric acid and HDLC, glucose and total cholesterol, triglycerides, LDL-C,
and VLDL-C.[3]
Our study showed that PCOS women had higher BMI,
significantly increased total cholesterol, triglycerides,
LDL-C and VLDL-C. On the other hand, serum levels of
HDL-C were significantly lower in this group compared
to controls.

CONCLUSION
The use of these simple biochemical parameters might
prove to be biomarkers in early detection of these
metabolic changes and may help to identify women
with PCOS at risk of cardio metabolic syndrome. Based
on early recognition of PCOS, efforts may be done to
limit or forestall the onset or progression of clinical
symptomatology. In addition, treatment may be
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Int J Clin and Biomed Res. 2016;2(4): 01-06

instituted in an attempt to prevent or restrict the longterm complications of PCOS namely diabetes and its
related complications, including cardiovascular disease.
However future prospective studies needed in this
aspect. Currently the most effective modalities appear
to be life-style modification and ovarian suppression by
oral contraceptives.
Acknowledgement
We extend special thanks to all the patients and
volunteers who took part in the study, for their kind cooperation.

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